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Circadian impact of psychosocial fac...
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Haynes, Patricia Lynn.
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Circadian impact of psychosocial factors in depression.
紀錄類型:
書目-電子資源 : Monograph/item
正題名/作者:
Circadian impact of psychosocial factors in depression./
作者:
Haynes, Patricia Lynn.
面頁冊數:
252 p.
附註:
Source: Dissertation Abstracts International, Volume: 64-06, Section: B, page: 2920.
Contained By:
Dissertation Abstracts International64-06B.
標題:
Psychology, Clinical. -
電子資源:
http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3094609
ISBN:
049642310X
Circadian impact of psychosocial factors in depression.
Haynes, Patricia Lynn.
Circadian impact of psychosocial factors in depression.
- 252 p.
Source: Dissertation Abstracts International, Volume: 64-06, Section: B, page: 2920.
Thesis (Ph.D.)--University of California, San Diego, 2003.
Severe life events increase the risk for major depression, and depression is associated with disrupted sleep. However, the impact of life stress on sleep has not been explored in individuals with unipolar depression. This project examined the proposed association between stressful life events and sleep using the social rhythm hypothesis of depression. Specifically, I tested whether participants with depression, when compared to normal controls, have: (a) less stable social rhythms (i.e., less consistent daily routines) that are more reactive to life stress, (b) a greater disruption of daily sleep and activity following life stress, (c) greater reactivity of sleep and daytime activity to disrupted social rhythms, (d) less light exposure, disrupted sleep, and increased daytime motor activity.
ISBN: 049642310XSubjects--Topical Terms:
524864
Psychology, Clinical.
Circadian impact of psychosocial factors in depression.
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Severe life events increase the risk for major depression, and depression is associated with disrupted sleep. However, the impact of life stress on sleep has not been explored in individuals with unipolar depression. This project examined the proposed association between stressful life events and sleep using the social rhythm hypothesis of depression. Specifically, I tested whether participants with depression, when compared to normal controls, have: (a) less stable social rhythms (i.e., less consistent daily routines) that are more reactive to life stress, (b) a greater disruption of daily sleep and activity following life stress, (c) greater reactivity of sleep and daytime activity to disrupted social rhythms, (d) less light exposure, disrupted sleep, and increased daytime motor activity.
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Thirty nine normal controls and 39 depressed individuals participated in the study. Over the course of two weeks, project staff gathered actigraphic estimates of motor activity and light exposure, prospective, daily measures of social interactions, and interview information about life events occurring in the previous 4 months. Data were analyzed by logistic and linear regression techniques. Results demonstrated that the presence of an event hypothesized to disrupt social rhythms in the last four months correlated with disrupted sleep continuity in depressed individuals but not in normal controls. In depressed individuals only, decreased sleep continuity was associated with fewer, daily, structured activities, especially those activities with others actively involved. Individuals experiencing decreased sleep continuity, low daytime light exposure, high in-bed (nighttime) light exposure, and a later activity acrophase had an increased likelihood of being depressed. In addition, individuals with more variable routines characterized by less active involvement with others were likely to be depressed. These findings are consistent with the proposed model in that individuals with depression experience more sleep disruption in response to life stress than non-depressed individuals. At the same time, daily routine does not appear to mediate the relationship between life stress and sleep. Future studies are needed to determine whether this sensitivity to life stress precedes the development of depression, thereby indicating a potential risk factor or etiological mechanism in the development of this disorder.
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